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Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study

AIM: To characterize the effect of hepatic steatosis (HS) on the progression of chronic hepatitis B. METHODS: A total of 162 chronic hepatitis B (CHB) patients confirmed by liver biopsy were involved in this study. All subjects were prospectively followed-up for 5 years in real-life clinical practic...

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Autores principales: Chen, Yangqin, Fan, Chunlei, Chen, Yuhan, Liu, Hui, Wang, Shanshan, Dong, Peiling, Li, Lei, Ding, Huiguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601678/
https://www.ncbi.nlm.nih.gov/pubmed/28938582
http://dx.doi.org/10.18632/oncotarget.17380
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author Chen, Yangqin
Fan, Chunlei
Chen, Yuhan
Liu, Hui
Wang, Shanshan
Dong, Peiling
Li, Lei
Ding, Huiguo
author_facet Chen, Yangqin
Fan, Chunlei
Chen, Yuhan
Liu, Hui
Wang, Shanshan
Dong, Peiling
Li, Lei
Ding, Huiguo
author_sort Chen, Yangqin
collection PubMed
description AIM: To characterize the effect of hepatic steatosis (HS) on the progression of chronic hepatitis B. METHODS: A total of 162 chronic hepatitis B (CHB) patients confirmed by liver biopsy were involved in this study. All subjects were prospectively followed-up for 5 years in real-life clinical practice. Fibrosis stage was determined using aspartate aminotransferase-to-platelet ratio index (APRI). The end-point was cirrhosis, liver cancer or death. The effects of steatosis on the biological behavior of hepatocellular carcinoma cells were investigated using oleic acid-induced lipid accumulation in HepG(2), HLE, PLC, and SMMC-7721 cells. RESULTS: Mean age, body mass index, and serum cholesterol were significantly higher in CHB patients with HS than those without HS at baseline (p< 0.05). The APRI was lower in patients without HS at baseline (p<0.05). Compared to patients with HS, APRI of patients without HS decreased significantly during the follow-up period (p<0.05). The 5-year cumulative incidence of cirrhosis were 4.17% and 5.19% in patients without and with HS, respectively (p>0.05). The multivariate analysis showed that older (RR 1.07, 95% CI 0.996-1.149, p = 0.065) and S3 stage of liver fibrosis (RR 3.50, 95% CI 0.812–15.117, p=0.093) were risk factors for the progression to cirrhosis. In vitro, cell steatosis promoted proliferation and migration of HCC cells and conferred cell cycle at S phase. CONCLUSION: The older and S3 stage of fibrosis may be risk factors for progression to cirrhosis in CHB patients with HS. HS may aggravate liver disease, promoting HCC progression.
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spelling pubmed-56016782017-09-21 Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study Chen, Yangqin Fan, Chunlei Chen, Yuhan Liu, Hui Wang, Shanshan Dong, Peiling Li, Lei Ding, Huiguo Oncotarget Research Paper AIM: To characterize the effect of hepatic steatosis (HS) on the progression of chronic hepatitis B. METHODS: A total of 162 chronic hepatitis B (CHB) patients confirmed by liver biopsy were involved in this study. All subjects were prospectively followed-up for 5 years in real-life clinical practice. Fibrosis stage was determined using aspartate aminotransferase-to-platelet ratio index (APRI). The end-point was cirrhosis, liver cancer or death. The effects of steatosis on the biological behavior of hepatocellular carcinoma cells were investigated using oleic acid-induced lipid accumulation in HepG(2), HLE, PLC, and SMMC-7721 cells. RESULTS: Mean age, body mass index, and serum cholesterol were significantly higher in CHB patients with HS than those without HS at baseline (p< 0.05). The APRI was lower in patients without HS at baseline (p<0.05). Compared to patients with HS, APRI of patients without HS decreased significantly during the follow-up period (p<0.05). The 5-year cumulative incidence of cirrhosis were 4.17% and 5.19% in patients without and with HS, respectively (p>0.05). The multivariate analysis showed that older (RR 1.07, 95% CI 0.996-1.149, p = 0.065) and S3 stage of liver fibrosis (RR 3.50, 95% CI 0.812–15.117, p=0.093) were risk factors for the progression to cirrhosis. In vitro, cell steatosis promoted proliferation and migration of HCC cells and conferred cell cycle at S phase. CONCLUSION: The older and S3 stage of fibrosis may be risk factors for progression to cirrhosis in CHB patients with HS. HS may aggravate liver disease, promoting HCC progression. Impact Journals LLC 2017-04-24 /pmc/articles/PMC5601678/ /pubmed/28938582 http://dx.doi.org/10.18632/oncotarget.17380 Text en Copyright: © 2017 Chen et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Chen, Yangqin
Fan, Chunlei
Chen, Yuhan
Liu, Hui
Wang, Shanshan
Dong, Peiling
Li, Lei
Ding, Huiguo
Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title_full Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title_fullStr Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title_full_unstemmed Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title_short Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study
title_sort effect of hepatic steatosis on the progression of chronic hepatitis b: a prospective cohort and in vitro study
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601678/
https://www.ncbi.nlm.nih.gov/pubmed/28938582
http://dx.doi.org/10.18632/oncotarget.17380
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